Ventricular tachycardia
Ventricular tachycardia is the rapid operation of the ventricles with a stroke rate of more than a hundred as a result of a foci that generates and maintains frequent electrical impulses. The symptomatology of ventricular tachycardia is dependent on its duration and can be manifested as an absolute absence of palpitation, and the development of collapse, as well as the onset of a lethal outcome.
The ventricular tachycardia can be established using an electrocardiogram. To treat ventricular tachycardia, antiarrhythmic drugs and cardioversion are used, which are prescribed according to the indications. If necessary, prolonged therapy with the use of a cardioverter defibrillator.
Arrhythmia, which is characterized by a frequency of contractions of the ventricles with a smaller rhythm, is called slow ventricular tachycardia. Such a condition is considered benign, so it does not need the use of drug treatment, until the hemodynamic symptoms appear.
The occurrence of ventricular tachycardia can be significantly affected by various cardiac abnormalities, as well as hypomagnesemia, hypokalemia, hypoxia, acidosis and the side effects of certain medications. This arrhythmia also occurs in several species, such as monomorphic, polymorphic, stable and unstable. Very often it grows into a ventricular fibrillation, and in the future this causes a cardiac arrest.
Paroxysmal ventricular tachycardia
This peculiar arrhythmia, which is characterized by paroxysms, that is, strokes of heart beat, not exceeding, as a rule, one hundred and eighty beats per minute is a paroxysmal ventricular tachycardia. These cardiac contractions occur as a result of impulses of an ectopic nature, which subsequently replace the normal sinus rhythm.
For paroxysmal ventricular tachycardia, a rapid onset and rapid termination, a varying duration, at which a constant rhythm is maintained, is characteristic. Ectopic tremors can form in the ventricles, atrioventricular junction or atria.
This form of arrhythmia in its etiology and pathogenetics is very similar to extrasystole. Thus, extrasystoles, following one after another, are regarded as a short attack of tachycardia. In this state, the circulation in the heart circulates ineffectively, therefore, palpitations, which are formed due to cardiac pathology, cause circulatory failure. When a prolonged ECG is performed in almost 25% of patients, a paroxysmal form of ventricular arrhythmia is revealed.
This arrhythmia is classified by location into forms such as ventricular, atrioventricular and atrial. The first two arrhythmias are combined and represent the supraventricular form. And here the paroxysmal ventricular tachycardia can proceed acutely, chronically and continuously recurring. The last form of arrhythmia can last for many years and cause at the same time arrhythmogenic cardiomyopathy, as well as circulatory insufficiency.
Depending on the mechanism of development of this form of tachycardia, it can be reciprocal, ectopic, multifocus and it is always preceded by extrasystole.
As a rule, the causes of paroxysmal tachycardia are increased activation of the sympathetic part of the nervous system and various defeats of the heart muscle in the form of inflammation, necrosis, dystrophy or sclerosis.
Paroxysmal ventricular tachycardia is characterized by ectopic excitations that are localized in the bundle of the Hyis, in the Purkinje fibers and the legs of the bundle of His. Most ventricular tachycardia develops more often in elderly men with coronary heart disease, hypertension, heart defects, myocarditis and heart attacks.
An important moment in the development of paroxysmal ventricular tachycardia is considered to be available additional ways for carrying out arousal in the myocardium with a congenital etiology or arising after myocarditis, cardiomyopathy or a heart attack. Such pathways cause a pathological cycle of excitations along the myocardium.
Symptomatic attacks with paroxysmal ventricular tachycardia can result from noise in the head, dizziness and a feeling of compressed heart. Hemiparesis and aphasia are less common. Sometimes there is sweating, nausea, flatulence and light subfebrile condition. At the end of the attack there is a prolonged polyuria in the form of a significant amount of urine of low density and with a light tint. Prolonged state of paroxysm can cause a decrease in blood pressure, weakness and development of fainting. For a paroxysmal ventricular tachycardia with a heart rate of more than one hundred and eighty beats per minute, the formation of ventricular fibrillation is characteristic.
Prolonged seizure may cause pulmonary edema and cardiogenic shock. Paroxysmal ventricular tachycardia is characterized by a change and expansion of the entire QRS complex, which resembles ventricular extrasystoles. Also, an unchanged, regular P-tooth can be detected on the electrocardiogram.
As a rule, patients with a diagnosis of paroxysmal ventricular tachycardia are urgently hospitalized. To stop paroxysm, Novokainamid, Propranolol, Aimalin, Quinidine, Rhythmodan, Cordarone, Isoptin and Etmozin are intravenously injected.
The prognosis of paroxysmal ventricular tachycardia is unfavorable, especially if it develops in cardiac pathologies, since such heart muscle lesions contribute to the formation of ventricular fibrillation. But in the absence of characteristic complications, patients achieve long-term survival.
Lethal outcome in this case is observed in patients with concomitant cardiac defects, as well as after previous clinical death or resuscitation.
Ventricular tachycardia causes
Ventricular tachycardia develops against a background of pathological heart disease and most often in the elderly after myocardial infarction. The younger generation is characterized by other diseases, such as cardiomyopathy of various forms( arrhythmogenic right ventricular, dilated, hypertrophic), as well as Brugada syndrome, myocarditis, heart defects and syndrome, which is characterized by an elongated QT.
At an elevated pressure, arrhythmia develops as a result of pronounced ventricular enlargement on the left and its expansion in combination with coronary insufficiency.
Very often, ventricular tachycardia is detected in the course of surgery performed in the chest, pericardial puncture, during endoscopy or cardiac catheterization. This may be due to mechanical irritation of the heart muscle, and is also a consequence of surgical intervention, anesthesia and hypoxia.
In addition, hypokalemia, poisoning with cyclopropane, chloroform may cause ventricular tachycardia. Also certain medications such as Alupet, Noradrenaline and Adrenaline and even Etmozin, Novokainamid, Quinidine( antiarrhythmic drugs) can cause tachycardia or make it much worse. It is rare to observe a gastric tachycardia without obvious defeats of the heart. Typically, this occurs in childhood or a little older, and the cause of this state remains unclear.
Sometimes this kind of arrhythmia can provoke some drugs that prolong the QT interval( Punctate, aminoglycosides, tricyclic antidepressants) or cause hypokalemia, i.e. Diuretics.
Factors that contribute to the onset of gastric tachycardia are various physical or mental stresses, smoking, hypokalemia, hypoxia, and disorders of acid and alkaline balance in the body.
Ventricular tachycardia symptoms
In different patients, ventricular tachycardia in its subjective sensations is not the same. Short-term seizures can greatly affect the overall well-being and therefore are determined only by ECG studies.
The symptomatology of the sensations is reminiscent of the sudden onset of attacks of heartbeat, which also end unexpectedly. Sometimes the ventricular tachycardia manifests itself in the form of a beginning weakness in the entire body, shortness of breath, the appearance of pain or heaviness behind the chest. But in some cases, there is a clinical picture, which is characterized by brain ischemia, ie, paresis, dizziness, aphasia, fainting, visual disturbances and Morgagni-Adams-Stokes syndrome, which is more often diagnosed in patients with atrial and ventricular blockade.
Attacks with ventricular tachycardia are very common and are manifested by cardiogenic shock and heart failure. Cardiogenic shock in ventricular tachycardia mainly occurs in patients with a diagnosis of myocardial infarction in acute form or with a stagnant form of heart failure. Sometimes arrhythmia provokes the development of pulmonary edema. During an attack, the heart rate can range from a hundred to two hundred beats per minute, and in some cases reaches even 300 strokes. As a rule, the ECG determines the right rhythm of the heart, but with prolonged observation it is possible to detect its irregularity.
When listening to the heart, there are loud fluctuations of the first tone, which is qualified as "cannon".It happens as a consequence of a short time( about 0.1 seconds) between an atrial systole and a ventricular systole.
Patients with lowered blood pressure are very poorly listened to the second heart tone, and sometimes it is almost impossible to hear, which can lead to erroneous calculation of cardiac contractions. Splitting of heart tones is associated with non-simultaneous contraction of the ventricles and the same closure of the valves. With ventricular tachycardia, the systole of the atria does not participate in the filling of the ventricles, so this reduces the cardiac output. And in the end it can cause collapse. In addition, the veins in the neck region have a smaller filling, in contrast to the pulsation of the arteries. This can be explained by the fact that the sinus node has control over the atrial systole. It is this symptom associated with the difference in pulsation, which is an important diagnostic criterion.
Other symptomatology and disorders will depend on the underlying pathology of the patient.
Ventricular tachycardia ECG
In the electrocardiogram, ventricular tachycardia manifests itself in the form of broadened QRS complexes that occur with a heart rate of more than one hundred beats per minute. At the time of an attack, the ventricular complexes may change or remain unchanged. Using these data, distinguish monomorphic ventricular tachycardia, bidirectional and ventricular tachycardia pirouette( polymorphic).
When pirouette, the QRS complex changes from one cycle to the next. With bi-directional tachycardia, not only the altered ventricular complex is noted, but also the change in the location of the electric axis of the heart. Thus, the right leg of the bundle is blocked, which alternates with the turns of the heart electroaxis to the left and to the right. With ventricular tachycardia, atrial contraction occurs regardless of the ventricles. Arrhythmia is recognized on the ECG when three consecutive ectopic complexes are detected, which follow with a heart rate of one hundred beats per minute. The duration of the attack can be more or less than thirty seconds, so the ventricular tachycardia is stable( > 30 seconds) and unstable( <30 seconds).An unstable form can be recognized during ECG monitoring during the day. A stable form very often provokes hemodynamic disorders, which contribute to the onset of ventricular fibrillation.
The heart rhythm with ventricular tachycardia is almost correct, and the atria contract independently of the ventricles.
Characteristic signs of ventricular tachycardia on ECG are: dissociation of atrioventicular character;QRS is greater than 0.14 seconds with the available ventricular complex as with blockade of the right bundle or more than 0.16 seconds as with blockade of the left branch of the bundle;Deviation of the cardiac electric axis to the left and ventricular complexes as in the blockade of the right leg of the bundle;Sharp deviation of the cardiac electric axis to the left by 90 degrees and QRS as in the blockade of the left leg of the bundle;The same direction of the complexes for all thoracic leads;Atypical form of QRS complexes.
Bi-directional ventricular tachycardia is characterized by an alternation of ventricular complexes located in two directions. The reason for such changes is not yet known. With the appearance of this form, arrhythmias on the ECG show severe myocardial damage or intoxication with cardiac glycosides. Her prognosis is very poor, as this leads to ventricular fibrillation.
For parasystolic, rare ventricular tachycardia, short paroxysms are characteristic. The first ectopic excitation is formed at different distances from the previous sine complex, that is, it manifests itself in the form of a non-constant coherence interval.
Ventricular pirouette or polymorphic tachycardia is a periodic change in the electroaxis of the ventricular complex, which leads to the appearance of negatively and positively directed complexes of QRS.In addition, the teeth R or S change in their amplitude, resembling a spindle. Hence the name of the form of ventricular tachycardia, which is characterized by absolute chaos in the formation of ventricular excitations. In addition, it is able to spontaneously cease. Very often, this form also has an extension of the QT interval caused by hypokalemia and hypomagnesemia.
Ventricular tachycardia treatment
All therapy of this condition is aimed at reducing heart rate and preventing further paroxysms with minimizing the occurrence of complications. As a rule, only malignant forms of arrhythmias need treatment. There are several indications for the use of antiarrhythmic drugs. For a start, this may be an unfavorable prognosis of ventricular tachycardia. Then its negative impact on hemodynamics and poor tolerance of arrhythmia.
In order to eliminate ventricular tachycardia, it is necessary to determine the source of its occurrence and, if possible, to try to get rid of it, especially if it is associated with mental and emotional reactions, various physical overstresses, parasympathetic effects, intoxications, arrhythmogenic effects of medications,
Persons who do not have chronic cardiac pathologies that do not tolerate ventricular extrasystole are prescribed psychotropic drugs. With bradycardia use anticholinergics, and in violation of the balance of electrolytes use drugs with magnesium and potassium.
To date, lidocaine is used to relieve paroxysmal ventricular tachycardia. Although it is considered not entirely effective, it acts quite quickly and causes minor complications. Also used during attacks are intravenous Novocainamide 10 mg / kg and Sotalol.
Antiarrhythmic drugs are prescribed for the treatment of tachycardia with non-coronary pathologies of the myocardium, for which its reduced contractile work is not characteristic. These drugs include Propafenone, Allapinin and Etatsizin.
A significant role in the treatment of ventricular tachycardia belongs to adrenergic blockers. These drugs reduce mortality in patients who have suffered a heart attack, as well as the frequency of sudden death.
Clinical studies suggest that the use of bisoprolol to treat patients with heart failure helps suppress arrhythmias and reduces mortality. In addition, it is safely used in heart diseases, which are combined with an increase in the ventricle on the left, the degeneration of the myocardium with various genesis and for the treatment of idiopathic ventricular tachycardia. Sometimes verapamil is used in therapy.
A fundamental role in the therapy of ventricular tachycardia is assigned to potassium channel blockers, which are characterized by a slowing of repolarization. Amiodarone, Sotalol, and some drugs not practiced in Russia, such as Azimilide, Ibutilide, Dofetilide, etc., are included in such drugs. However, studies have shown that Sotalol, having high efficiency, has many side effects, for example, arrhythmogenic effect and itsThe probability increases with raising the dose of this remedy.
Patients with polymorphic arrhythmia are treated with the size of QT on the sinus rhythm of the heart. With stable dynamics and the initially available normal QT interval, antiarrhythmics such as Amiodarone, Beta-blocker, Procainamide, Lidocaine, Sotalol are prescribed. With reduced myocardial contraction, therapy is limited to use in reduced doses of lidocaine, Amiodarone, or electrocardiovascular cardioversion.
Coupling of paroxysm for polymorphic arrhythmia, which is characterized by an elongated QT interval, is achieved by intravenous administration of Magnesia or by artificial imposition of a rhythm with a higher frequency. Sometimes a positive result can be achieved through the introduction of isoproterenol. Sometimes the appointment of lidocaine or diphenin is sufficient.
For those patients who experience cardiac or myocardial ischaemia during cardiac arrhythmia, pulmonary edema, or hypotension, electroshock is used at a rhythm frequency of one hundred and fifty beats per minute. Then the patients start to provide first aid in the form of oxygen supply, install a catheter into a vein and prepare a set for intubation. Before the therapy, the electro-pulses are administered calming diazepam up to 15 mg intravenously or Morphine, as a preparation for premedication. In patients with monomorphic arrhythmia, the attack can be controlled with a charge of energy of 100 j.
Recently, in practical medicine, implantation of cardioverter defibrillators has been widely used to reduce the risk of death of patients diagnosed with malignant forms of arrhythmia.
